A nuclear post-transcriptional mechanism mediates the induction of fibronectin by glucocorticoids

Ehretsmann, C P; Chandler, Lois A.; Bourgeois, Suzanne

doi:10.1016/0303-7207(95)03531-b

Cited by 16 publications

(8 citation statements)

References 38 publications

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“…Taken together, these observations may imply that transcription of leptin and splicing of its receptor are regulated by steroids. Thus, our hypothesis regarding a role for LTR5 in the control by steroids of alternative splicing, combined with previous data (Hayward-Lester et al 1996;Ehretsmann et al 1995;Norgren et al 1994;Cramer et al 1997;McCracken et al 1997;Shimizu et al 1997;Zachow and Magoffin 1997;Chehab et al 1996), suggests that the proportions of OBRa and OBRb forms of leptin receptor may be regulated by steroids, possibly through interaction with the LTR5 sequence. By using similar functional elements, LTR5 and MER11 may provide an evolutionary basis for the coordinate expression of leptin and its receptor.…”

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confidence: 71%

“…The transcription of LTR from another HERV-K-related retrovirus, murine mammary tumor virus (MMTV), is also activated by steroids (Le Ricousse et al 1996). Furthermore, it has been shown that glucocorticoid and progesterone may affect the posttranscriptional processing of various genes (Hayward-Lester et al 1996;Ehretsmann et al 1995) including alternative splicing of the human insulin receptor gene (Norgren et al 1994) in a dose-dependent way. Finally, it has been shown that splicing may depend on transcription (Cramer et al 1997;McCracken et al 1997).…”

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confidence: 99%

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The Long Terminal Repeat of an Endogenous Retrovirus Induces Alternative Splicing and Encodes an Additional Carboxy-Terminal Sequence in the Human Leptin Receptor

Kapitonov

Jurka

1999

J Mol Evol

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The evolution of mammalian protein structure and regulation, specifically transcriptional and posttranscriptional regulation, may include among its tools the use of abundant retroviral long terminal repeats (LTRs). In particular, LTRs may be turned into switches for alternative splicing. This type of regulatory pathway is illustrated by the alternative splicing in the human leptin receptor (OBR). The human leptin receptor is involved in the control of important biological processes including energy expenditure, production of sex hormones, and activation of hemopoietic cells. OBRa and OBRb are the two major, alternatively spliced forms of the leptin receptor, called the "short form" and the "long form," respectively. We report that the OBRa short form is the result of a double splicing event which occurs within the LTR of the endogenous retrovirus HERV-K. Working as a switch of alternative splicing, this LTR also encodes the terminal 67 amino acid residues in OBRa. We suggest the possibility of transcriptional and posttranscriptional regulation of OBR expression by steroids that bind the LTR.

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confidence: 71%

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confidence: 99%

The Long Terminal Repeat of an Endogenous Retrovirus Induces Alternative Splicing and Encodes an Additional Carboxy-Terminal Sequence in the Human Leptin Receptor

Kapitonov

Jurka

1999

J Mol Evol

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“…These include expression of fibronectin (71), alkaline phosphatase (72,73), interleukin-2 (74), tumor necrosis factor-␣ (75), peptidylglycine ␣-amidating monooxygenase (76), and spot 14 (61). Regulation of fibronectin expression by dexamethasone involves changes in pre-mRNA amounts without changes in transcription rate of the gene (71). In the case of the alkaline phosphatase gene, its pre-mRNA is only processed to mature mRNA when the cells are treated with retinoic acid (73).…”

Section: Discussionmentioning

confidence: 99%

Regulation of the Processing of Glucose-6-phosphate Dehydrogenase mRNA by Nutritional Status

Amir-Ahmady

Salati

2001

Journal of Biological Chemistry

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Expression of glucose-6-phosphate dehydrogenase (G6PD) gene during starvation and refeeding is regulated by a posttranscriptional mechanism occurring in the nucleus. The amount of G6PD mRNA at different stages of processing was measured in RNA isolated from the nuclear matrix fraction of mouse liver. This nuclear fraction contains nascent transcripts and RNA undergoing processing. Using a ribonuclease protection assay with probes that cross an exon-intron boundary in the G6PD transcript, the abundance of mRNAs that contain the intron (unspliced) and without the intron (spliced) was measured. Refeeding resulted in 6-and 8-fold increases in abundance of G6PD unspliced and spliced RNA, respectively, in the nuclear matrix fraction. However, the amount of G6PD unspliced RNA was at most 15% of the amount of spliced RNA. During refeeding, G6PD spliced RNA accumulated at a rate significantly greater than unspliced RNA. Further, the amount of partially spliced RNA exceeded the amount of unspliced RNA indicating that the enhanced accumulation occurs early in processing. Starvation and refeeding did not regulate either the rate of polyadenylation or the length of the poly(A) tail. Thus, the G6PD gene is regulated during refeeding by enhanced efficiency of splicing of its RNA, and this processing protects the mRNA from decay, a novel mechanism for nutritional regulation of gene expression.Glucose-6-phosphate dehydrogenase (G6PD, 1 EC 1.1.1.49) is the rate-limiting enzyme of the pentose phosphate pathway. All cells contain G6PD activity; however, nutritional and hormonal factors only regulate the expression of the enzyme in liver and adipose tissue (1-3). Regulation of G6PD activity in these tissues is because it plays a critical role in the de novo synthesis of fatty acids by providing 50 -75% of the NADPH for the fatty acid synthase reaction (4). Thus, G6PD is a member of the lipogenic enzyme family. The activities of the lipogenic enzymes are coordinately regulated so that flux of substrate through the fatty acid biosynthetic pathway is high when animals consume a diet rich in carbohydrate and flux is decreased by starvation or the addition of polyunsaturated fat to the diet (reviewed in Ref. 5). However, the molecular mechanisms causing these changes in flux vary considerably between enzymes.The enzymes of the fatty acid biosynthetic pathway are regulated at both transcriptional and posttranscriptional steps. Fatty acid synthase (6 -8), acetyl-CoA carboxylase (9, 10), stearoyl-CoA desaturase (11), and ATP-citrate lyase (12) undergo large changes in their transcriptional rates in response to dietary manipulations. Regulation of malic enzyme expression during a chow to fat-free diet transition occurs by changes in mRNA stability in the cytoplasm (13). In addition, cytoplasmic mRNA stability is also involved in the regulation of stearoylCoA desaturase expression by fatty acids in yeast (14) and in adipocytes (15). Posttranscriptional regulation is the primary mechanism involved in the nutritional regulation of G6PD expressi...

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“…Alternatively, the pattern of expression of GnRH nuclear mRNA may be a result of enhanced mRNA stability in the nucleus. These mechanisms have previously been reported in other systems [34, 35, 36], but never for GnRH. Nevertheless, this result suggests that changes in GnRH mRNA in the cytoplasm with time are probably determined by alterations at a posttranscriptional level in the nucleus, as opposed to a change in GnRH mRNA stability in the cytoplasm, and levels of GnRH mRNA in the cytoplasm may reflect steady-state transport of mature GnRH mRNA molecules out of the nucleus.…”

Section: Discussionmentioning

confidence: 74%

Diurnal Rhythmicity of Gonadotropin-Releasing Hormone Gene Expression in the Rat

Gore

1998

Neuroendocrinology

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The release of the decapeptide gonadotropin-releasing hormone (GnRH) from neuroterminals in the median eminence varies depending upon the stage of development, time of day, reproductive season, and day of the ovarian cycle. With respect to the biosynthetic events responsible for such alterations in GnRH release, we have reported that increases in GnRH mRNA occur concomitantly with or precede the proestrous GnRH/LH surge in female rats, and the pubertal increase in GnRH. Because a hallmark of puberty is the development of nocturnal increases in gonadotropin/GnRH release, in the present study, we examined whether a rhythm in GnRH gene expression occurs that may be responsible for this rhythm of neurosecretion. Additionally, we extended the previous finding of diurnal rhythms of GnRH gene expression in cycling females to adult male rats. The mechanism for these changes, i.e. GnRH gene transcription, RNA processing or a posttranscriptional mechanisms was also elucidated. In experiment I, GnRH gene expression was measured in female rats at different stages of puberty [P25 (juvenile); ∼P37 (day of vaginal opening); and P45 (postpubertal)] at 10.00, 14.00, 18.00, 22.00, 2.00 and 6.00 h. GnRH mRNA levels increased significantly during pubertal development, independent of any changes in GnRH gene transcription or RNA processing, indicating a posttranscriptional mechanism. GnRH mRNA levels did not vary with time of day in these pubertal rats, indicating that the diurnal rhythm of GnRH release that develops during puberty is probably a posttranslational event. In experiment II, GnRH gene expression was measured in adult male rats at the same 4-hour intervals. GnRH mRNA levels varied significantly with time of day: they increased from 10.00 to 14.00 h, remained elevated through 22.00 h, then decreased significantly to the nadir at 10.00 h. The mechanism for these changes appears to involve processing or stability of the GnRH mRNA in the nucleus. These results indicate that GnRH mRNA levels are regulated differentially with time of day depending upon age and gender.

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A nuclear post-transcriptional mechanism mediates the induction of fibronectin by glucocorticoids

Cited by 16 publications

References 38 publications

The Long Terminal Repeat of an Endogenous Retrovirus Induces Alternative Splicing and Encodes an Additional Carboxy-Terminal Sequence in the Human Leptin Receptor

The Long Terminal Repeat of an Endogenous Retrovirus Induces Alternative Splicing and Encodes an Additional Carboxy-Terminal Sequence in the Human Leptin Receptor

Regulation of the Processing of Glucose-6-phosphate Dehydrogenase mRNA by Nutritional Status

Diurnal Rhythmicity of Gonadotropin-Releasing Hormone Gene Expression in the Rat

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